Παρ΄όλο ότι πρόκειται για αναχαιτιζόμενες παθήσεις, τα νεοπλάσματα του πνεύμονος παραμένουν η πρώτη αιτία θανάτου από νεοπλάσματα στους άνδρες, και η δεύτερη στις γυναίκες, αφού προσβάλλοιυν εκατοντάδες χιλιάδες κάθε χρόνο. η επιδημιολογική διασπορά της παθήσεως εμφανίστηκε 20 χρόνια μετά τη βιομηχανική παραγωγή του τσιγάρου και την ευρεία διάδοση της καπνιστικής συνήθειας, από το 1900 για τους άνδρες και από το 1920, για τις γυναίκες. Κατά το 1940, περίπου 70% των ανδρών και 40% των γυναικών ήταν καπνιστές. Η μελέτη των Doll και Hill, to 1950, έδειξε την αιτιολογική σχέση του καπνίσματος με τα νεοπλάσματα του πνεύμονος. Ο κίνδυνος προσβολής από βρογχογενές καρκίνωμα αναγνωρίσθηκε ανάλογος του αριθμού των ημερησίως καπνιζόμενων τσιγάρων και του καπνιστικού ιστορικού (διάρκεια, συχνότητα). Έτσι, ένα καπνιστής 30 τσιγάρων την ημέρα διατρέχει 30 φορές μεγαλύτερο κίνδυνο να καταλήξιε από βρογχογενές καρκίνωμα, συγκτιτικά με έναν μη καπνιστή. Επί διακοπής του καπνίσματος, ο κίνδυνος υποδιπλασιάζετια, κάθε 5 χρόνια αποχής. Η δημοφιλία του καπνίσματος έχει μειωθεί τα τελευταία χρόνια, έτσι, που σήμερα, μόνο 29% των ανδρών και 28% των γυναικαών είναι συστηματικοί καπνιστές, ενώ, επίσης, οι επιδημιολογικοί δείκτες του βρογχογενούς καρκινώματος έχουν αρχίσει να μειώνονται, τόσο στους άνδρες, όσο και στις νεότερες γυναίκες, αν και εξακολουθούν να εμφανίζονται υψηλοί δείκτες στις ηλιωμένες γυναίκες. Η καπνιστική συνήθεια κυμαίνεται από χώρα σε χώρα. Ο κίνδυνος του καρκίνου σε πρώην καπνιστές παραμένει υψηλότερος, συγκριτικά με τους μη καπνιστές, ακόμη και 40 χρόνια μετά τη διακοπή του. Έτσι, ο μόνος αποτελεσματικός τρόπος μειώσεως της επιπτώσεως του βρογχογενούς καρκίνου είναι η πλήρης αποχή από το κάπνισμα.
Το παθητικό κάπνισμα είναι, επίσης, αίτιο βρογχογενούς ακρκινώματος. Π.χ., μια γυναίκα που δεν κάπνισε ποτέ, έχει ένα εκτιμούμενο κίνδυνο να καταλήξει από καρκίνο του πνεύμονος 24% μεγαλύτερο, ως σύζυγος καπνιστού, από μια άλλη μη καπνίστρια η οποία είναι σύζυγος μη καπνιστού. Γενετικοί παράγοντες, διαδραματίζουν σημαντικό ρόλο στην επηρρέπεια προσβολής των καπνιστών, αλλά και στην υιοθέτηση του τρόπου ζωής (κάπνισμα). Επίσης, είναι γνωστό ότι ο βαθμός επαγωγής της υδροξυλάσης των αρυλ-υδοργονανθράκων μκπορεί να καθορίζεται γενετικά και να ενεργοποιούν τους υδοργονάνθρακες του καπνού προς καρκινογόνα. Επίσης, υπάρχει αυξημένη επίπτωση καρκίνου μεταξύ ασθενών με πνευμονική ίνωση όπως η κρυπτογενής ινώδης κυψελιδίτις, το σκληρόδερμα, ενώ το καλούμενο ”scar carcinoma, ουλώδες καρκίνωμα” παρατηρείται σε περιοχές, που προϋπάρεχουν ουλές από παληά φυματίωση.
Μερικές μελέτες υποστηρίζουν ότι η διατροφή παίζει σημαντικό ρόλο, στη διαμόρφωση των επιδημιολογικών δεικτών του καρκίνου και η καθημερινή λήψη αρκετών ποσοτήτων φρούτων, λαχανικών που περιέχουν β-καροτένιο, μειώνει τον κίνδυνο του καρκίνου. Η έκθεση σε ιονίζουσα ακτινοβολία όπως η προερχόμενη από το ραδόνιο, που εκπέμπεται από το έδαφος και τα υλικά οικοδομών, μπορεί να έχει επιδημιολογική σημασία, ιδιαίτερα στην επίπτωση βρογχογενούς καρκινώματος επί μη καπνιστών. Η επαγγελματική επίπτωση στον αμίαντο αυξάνει τον κίνδυνο προσβολής και φαίνεται ότι υπάρχει ευθεία συσχέτιση της δόσεως με της προσβολής. Επιπλέον, η συνύπαρξη καπνίσματος και αμιάντου είναι πολλαπλασιατική.
Η επαγγελματική έκθεση και το οικογενειακό ιστορικό προσβολών σε μικρή ηλικία συγκαταλέγονται μεταξύ των σοβαρών παραγόντων κινδύνου καρκινογενέσεως, μεταξύ μη καπνιστών (►).
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